From where is aldosterone (a hormone) secreted and what is its primary function in the body?

Aldosterone Secretion and Function

Aldosterone is secreted from the zona glomerulosa of the adrenal cortex and functions primarily to regulate sodium homeostasis and blood pressure by promoting sodium reabsorption in the renal collecting duct. 1, 2

Site of Secretion

• Aldosterone is synthesized and secreted exclusively from the zona glomerulosa, the outermost layer of the adrenal cortex. 2, 3
• This specialized region of the adrenal gland is distinct from other cortical zones and is responsible for mineralocorticoid production. 2

Primary Physiological Functions

Sodium and Volume Regulation

• Aldosterone's principal action is to increase sodium reabsorption in the renal cortical collecting duct through upregulation of the epithelial sodium channel (ENaC). 1, 4
• This sodium retention leads to water reabsorption and expansion of extracellular fluid volume, which directly increases blood pressure. 1, 5, 4
• The hormone also promotes potassium and hydrogen ion excretion in exchange for sodium reabsorption, which can lead to hypokalemia and metabolic alkalosis when aldosterone is excessive. 5, 3

Blood Pressure Control

• By regulating sodium homeostasis, aldosterone serves as a critical controller of blood volume and blood pressure. 2, 4
• The expanded fluid volume from sodium retention increases effective circulating volume and elevates blood pressure through hemodynamic mechanisms. 5

Regulatory Mechanisms

Primary Controllers

• The renin-angiotensin-aldosterone system (RAAS) is the dominant regulator of aldosterone secretion, with angiotensin II being the most potent stimulus. 2, 6, 4
• Serum potassium concentration is the second major regulator—elevated potassium directly stimulates aldosterone production from zona glomerulosa cells. 2, 6, 4
• Adrenocorticotropic hormone (ACTH) provides minor regulatory input to aldosterone secretion. 2, 3

Negative Feedback

• Under normal physiological conditions, aldosterone-induced volume expansion suppresses renin secretion, creating a negative feedback loop. 1
• This suppression of the entire renin-angiotensin cascade prevents excessive aldosterone production in healthy individuals. 1

Additional Non-Hypertensive Effects

• Beyond blood pressure regulation, aldosterone exerts direct toxic effects on cardiovascular tissues, including promotion of cardiac fibrosis, myocardial hypertrophy, vascular remodeling, endothelial dysfunction, and renal fibrosis. 7, 3
• These tissue effects occur through mineralocorticoid receptors expressed in cardiomyocytes, endothelial cells, neurons, and other non-epithelial tissues. 7, 3
• Aldosterone excess causes disproportionately greater cardiovascular damage than hypertension alone, with dramatically increased risks of heart failure (3.7-fold), stroke (4.2-fold), myocardial infarction (6.5-fold), and atrial fibrillation (12.1-fold). 8

Clinical Significance

Pathological States

• Insufficient aldosterone secretion leads to hypotension and circulatory shock, particularly dangerous in infancy. 2
• Excessive aldosterone production (primary aldosteronism) causes hypertension that is resistant to standard therapy and carries substantially higher cardiovascular risk than essential hypertension. 9, 8
• Primary aldosteronism affects 5-10% of all hypertensive patients and up to 20% of those with resistant hypertension, making it the most common endocrine cause of hypertension. 9, 8

Mechanism of Action

• Aldosterone acts through both genomic and non-genomic pathways by binding to cytosolic mineralocorticoid receptors that translocate to the nucleus and modulate gene expression. 3
• The genomic effects induce transcription of proteins involved in sodium transport, while rapid non-genomic actions occur in epithelial and non-epithelial tissues. 3